Abi1 loss drives prostate tumorigenesis through activation of EMT and non-canonical WNT signaling.

ABSTRACT:

Background

Prostate cancer development involves various mechanisms, which are poorly understood but pointing to epithelial mesenchymal transition (EMT) as the key mechanism in progression to metastatic disease. ABI1, a member of WAVE complex and actin cytoskeleton regulator and adaptor protein, acts as tumor suppressor in prostate cancer but the role of ABI1 in EMT is not clear.

Methods

To investigate the molecular mechanism by which loss of ABI1 contributes to tumor progression, we disrupted the ABI1 gene in the benign prostate epithelial RWPE-1 cell line and determined its phenotype. Levels of ABI1 expression in prostate organoid tumor cell lines was evaluated by Western blotting and RNA sequencing. ABI1 expression and its association with prostate tumor grade was evaluate

SUBMITTER: Nath D 

PROVIDER: S-EPMC6749699 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature